Retinoic acid (RA) receptor transcriptional activation correlates with inhibition of 12-O-tetradecanoylphorbol- 13-acetate-induced ornithine decarboxylase (ODC) activity by retinoids: A potential role fortrans-RA-induced ZBP-89 in ODC inhibition

Dawson, Marcia I.; Park, Ju Hui; Chen, Guo Quan; Chao, Wan Ru; Dousman, Linda; Waleh, Nahid; Hobbs, Peter D.; Jong, Ling; Toll, Lawrence; Zhang, Xiao Kun; Gu, Jingmin; Agadir, Anissa; Merchant, Juanita L.; Bai, Longchuan; Verma, Ajit Kumar; Thacher, Scott M.; Chandraratna, Roshantha A.S.; Shroot, Braham; Hill, Donald L.

doi:10.1002/1097-0215(20010101)91:1<8::aid-ijc1007>3.0.co;2-h

Cited by 19 publications

(9 citation statements)

References 44 publications

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“…The anti‐inflammatory effects of retinoids, known to be mediated in part by anti‐AP‐1 activity, were evaluated in the TPA‐induced ear oedema mouse model . All tested compounds, including the RARγ‐selective agonist trifarotene, showed potent anti‐inflammatory characteristics in vivo , resulting in ear oedema reduction of 73%, 99% and 95% for trifarotene, tazarotene and tazarotenic acid, respectively (Fig.…”

Section: Resultsmentioning

confidence: 99%

Nonclinical and human pharmacology of the potent and selective topical retinoic acid receptor-γ agonist trifarotene

et al. 2018

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Section: Resultsmentioning

confidence: 99%

Nonclinical and human pharmacology of the potent and selective topical retinoic acid receptor-γ agonist trifarotene

et al. 2018

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“…For the rat pituitary adenoma cell line GH4, we showed that elevated expression of ZBP-89 inhibits cell proliferation (39). ZBP-89 expression is significantly induced by trans-retinoic acid or butyrate, which also induces terminal differentiation of a colon cancer cell line (5,9). Moreover, we recently found that ZBP-89 cooperates with p300 to potentiate the butyrate-induced activation of p21 waf1 (5).…”

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confidence: 96%

ZBP-89 Promotes Growth Arrest through Stabilization of p53

Bai¹,

Merchant

2001

Molecular and Cellular Biology

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102

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Transcription factor p53 can induce growth arrest and/or apoptosis in cells through activation or repression of downstream target genes. Recently, we reported that ZBP-89 cooperates with histone acetyltransferase coactivator p300 in the regulation of p21 waf1 , a cyclin-dependent kinase inhibitor whose associated gene is a target gene of p53. Therefore, we examined whether ZBP-89 might also inhibit cell growth by activating p53. In the present study, we demonstrate that elevated levels of ZBP-89 induce growth arrest and apoptosis in human gastrointestinal cell lines. The ZBP-89 protein accumulated within 4 h, and the p53 protein accumulated within 16 h, of serum starvation without changes in p14ARF levels, demonstrating a physiological increase in the cellular levels of these two proteins. Overexpression of ZBP-89 stabilized the p53 protein and enhanced its transcriptional activity through direct protein-protein interactions. The DNA binding and Cterminal domains of p53 and the zinc finger domain of ZBP-89 mediated the interaction. A point mutation in the p53 DNA binding domain, R273H, greatly reduced ZBP-89-mediated stabilization but not their physical interaction. Furthermore, ZBP-89 formed a complex with p53 and MDM2 and therefore did not prevent the MDM2-p53 interaction. However, heterokaryon assays demonstrated that ZBP-89 retained p53 in the nucleus. Collectively, these data indicate that ZBP-89 regulates cell proliferation in part through its ability to directly bind the p53 protein and retard its nuclear export. Our findings further our understanding of how ZBP-89 modulates cell proliferation and reveals a novel mechanism by which the p53 protein is stabilized.

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“…It has been shown to interact with p53 and stabilize it, thus contributing to apoptosis [36]. Its expression is induced by butyrate [37], retinoic acid [38] and TGF-β [35], and we have seen a decrease in mRNA expression in fibroblasts in response to inflammatory cytokines (data not shown). Recent evidence suggests post-translational regulation occurs as well [39].…”

Section: Discussionmentioning

confidence: 65%

NF-κB and ZBP-89 regulate MMP-3 expression via a polymorphic site in the promoter

Borghaei

Gorski

Javadi

et al. 2009

Biochemical and Biophysical Research Communications

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A 5T/6T polymorphism in the human MMP-3 promoter affects gene expression and impacts the risk and/or severity of various pathological conditions. Chromatin immunoprecipitation (ChIP) in human fibroblasts homozygous for the 6T site demonstrate that it is bound by NF-κB and ZBP-89 transcription factors in its native chromatin. ChIP in COS-1 cells transfected with plasmids containing the 5T and 6T sites in the context of 2 kb of the MMP-3 promoter showed that NF-κB p50 binds preferentially to the 6T site, while more ZBP-89 binding is detected to the 5T site. Over-expressed ZBP-89 increased transcription from the 5T promoter but not from the 6T, while NF-κB decreased transcription from both promoters, even in the presence of excess ZBP-89. A model is suggested in which the physiological impact of the polymorphism is dependent on the relative levels and activities of these competing factors in various cell types and conditions.

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Retinoic acid (RA) receptor transcriptional activation correlates with inhibition of 12-O-tetradecanoylphorbol- 13-acetate-induced ornithine decarboxylase (ODC) activity by retinoids: A potential role fortrans-RA-induced ZBP-89 in ODC inhibition

Cited by 19 publications

References 44 publications

Nonclinical and human pharmacology of the potent and selective topical retinoic acid receptor-γ agonist trifarotene

Nonclinical and human pharmacology of the potent and selective topical retinoic acid receptor-γ agonist trifarotene

ZBP-89 Promotes Growth Arrest through Stabilization of p53

NF-κB and ZBP-89 regulate MMP-3 expression via a polymorphic site in the promoter

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